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human physiology > human phys exam 2 > Flashcards

human phys exam 2 Flashcards

1
Q

types of muscles

A

skeletal
cardiac
smooth

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2
Q

skeletal muscles

A

large
multinucleate
one muscle fiber
voluntary muscle controlled by somatic efferent neurons

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3
Q

cardiac muscles

A

smaller than skeletal
uninucleate
striated
all cells are connected by intercalated disks
involuntary muscle controlled by autonomic motor neurons

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4
Q

smooth muscle

A

small
no striations
uninucleate
involuntary muscle controlled by autonomic motor neurons

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5
Q

muscle fiber

A

muscle cell
called syncitum

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6
Q

sarcolemma

A

cell membrane in skeletal muscle

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7
Q

sarcoplasm

A

cytoplasm in skeletal muscles

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8
Q

sarcoplasmic reticulum

A

endoplasmic reticulum in muscles
stores calcium

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9
Q

myofibrils

A

bundles of contractile proteins
each muscle fiber has myofibrils

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10
Q

contractile proteins in muscle fibers

A

actin
myosin
troponin
tropomyosin

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11
Q

actin

A

thin filament
5 nm

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12
Q

myosin

A

thick filament
15 nm

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13
Q

t- tubules

A

extensions of sarcolemma that associate with ends of sarcoplasmic reticulum
allows action potential to go deep into muscle

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14
Q

a band

A

anywhere there is myosin
(can be actin)

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15
Q

h zone

A

only myosin

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16
Q

i band

A

only actin

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17
Q

m line

A

where myosin is anchored

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18
Q

z disk

A

where actin is anchored

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19
Q

sarcomere

A

z disk to z disk
3 um in lenght

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20
Q

titin

A

huge protein
like a spring
gives passive tension to muscle

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21
Q

myosin molecule

A

each molecule has 2 myosin heads
hinge region allows molecule to pivot

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22
Q

during contraction
in sarcomere

A

sarcomere shortens
length of actin and myosin DO NOT change!
there is just more overlap between actin and myosin
- i band gets shorter
- h zone gets shorter

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23
Q

cross bridge cycle in skeletal muscle

A
  1. ATP binds to myosin, causes myosin to leave rigor state and unbind from actin
  2. myosin hydrolyzes (ATPase activity) ATP to ADP and inorganic phosphate (high energy state). This causes myosin hinge point to pivot
  3. myosin head swings over and binds weakly to a new molecule (high energy state). Release inorganic phosphate
  4. release of inorganic phosphate causes Power Stroke. myosin head rotates and pushes actin past it
  5. this causes sarcomer to get shorter
  6. end of power stroke, myosin releases ADP and is still binded to actin (rigor state)
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24
Q

what prevent cross bridge from happening
(why arent our muscles always contracting)

A

tropomyosin lays on top of binding site between actin and myosin, prevents myosin to bind to actin and complete power stroke
(this is after myosin hydrolyzes ATP)

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25
Q

How is tropomyosin moved to allow contraction?

A

when cytosilic calcium binds to troponin, it causes conformation change to troponin which pulls tropomyosin away from the binding site
this allows myosin to bind to actin and complete power stroke

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26
Q

excitation-contraction coupling

A
  1. somatic motor neurons release ACh
  2. Na+ enters through ACh receptor –> initiates action potential (depolarizes)
  3. action in t-tubule alters conformation of DHP receptor
  4. DHP opens Ryr Ca+ channels, releases Ca into cytoplasm
  5. Ca binds to troponin
  6. myosin completes power stroke
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27
Q

how does relaxation occur?
IN SKELETAL MUSCLES

A

calcium needs to be removed
1. Sarcoplasmic Ca-ATPase (SERCA) pumps calcium back into sarcoplasmic reticulum against concentration gradient
2. decrease in calcium causes calcium to unbind from troponin
3. tropomyosin can rebind to myosin binding site
relax

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28
Q

3 roles of ATP in skeletal muscle contraction

A
  1. myosin hydrolyzes ATP, provides energy for cross bridge
  2. binding of ATP to myosin dissociates actin and myosin
  3. hydrolysis of ATP by Ca-ATPase provides energy for active transport of calcium back into SR
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29
Q

motor unit

A

motor neuron and muscle fiber it innervates
- there are way more muscle fibers than neurons
- each muscle fiber is innervated by a single neuron
- each neuron innervates multiple muscle fibers

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30
Q

latent period

A

twitch is delayed from action potential because the time it takes for calcium to increase in sarcoplasm and interact with troponin
twitch contraction lasts longer than action potential because it takes time for calcium to pumped back into SR

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31
Q

temporal summation skeletal muscle

A

2 action potential stimuli are close in time, can cause a larger tiwitch
twitch lasts much longer than action potential

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32
Q

isotonic contraction

A

muscle moves the load and gets shorter

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33
Q

isometric contraction

A

muscle forces balances out the weight, so the muscle doesnt move the load

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34
Q

lengthening contraction

A

the weight wins, so despite the muscle trying to contract it still gets shorter

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35
Q

contraction steps

A
  1. muscle at rest
  2. isometric contraction: muscle hasn’t shortened (sarcomeres have shortened but elastic elements stretch = length is same)
  3. isotonic contraction (elastic components are fully stretched but still more overlap of actin and myosin = muscle shortens)
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36
Q

slow oxidative muscle fiber

A
  • darker because they contain myoglobin
  • use oxidative phosphorylation (lot of ATP)
  • resist muscle fatigue
  • small diameter: allow oxygen can go into muscle
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37
Q

fast oxidative muscle fiber

A
  • mediam diameter fibers
  • contain less myoglobin
  • can use glyolysis and oxidaive phosphorylation
  • produce greater amount of tension than slow but will fatigue (not as quickly as fast glycolytic)
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38
Q

muscle fiber recruitment

A

recruit fibers that are least energetically expensive (slow oxidative)

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39
Q

similarities between skeletal and smooth muscle

A

specialized for contraction
contract by sliding myosin and actin
calcium is important regulator
contraction requires ATP

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40
Q

single unit smooth muscle

A

gap junctions connect cytoplasm of 2 cells so ATP can travel
contract in synchronous because of gap junction

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41
Q

multi unit smooth muscle

A

not connected by gap junction but rather axons
more precise control

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42
Q

innervation of smooth muscle

A

autonomic nervous system
parasympathetic pathway
sympathatetic pathway
adrenal sympathetic pathway

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43
Q

innervation of skeletal muscle

A

somatic motor pathway

neuron releases acetylcholine, actins on nicotinic acetylcholine receptor (ligand gated) in skeletal muscle

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44
Q

parasympathetic innervation of smooth muscle

A

preganglionic: releases Ach acts on nicotininc receptor on ganglion
post ganglionic: releases Ach acts on g-protein (muscarinic)receptors in smooth muscle

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45
Q

sympathetic innervation of smooth muscle

A

preganglionic: releases Ach acts on nicotinic receptor on ganglion
postganglionic: releases norepinephrine acts on adrenergic receptors (g-coupled)

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46
Q

adrenal sympathetic innervation of smooth muscle

A

preganglionic: releases Ach acts on nicotinic receptors in adrenal medulla
releases epinephrine into bloodstream

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47
Q

dense bodies

A

where actin is anchored in smooth muscles
when smooth muscle contracts, they get closer to each other

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48
Q

contraction in smooth muscle

A
  1. Ca enters cell from SR
  2. Ca binds to calmodulin (CaM)
  3. CaM activates myosin light chain kinase (MLCK)
  4. MLCK phosphorylates light chain in myosin head –> increases myosin ATPase activity
  5. active myosin crossbridges slide along actin and create muscle tension
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49
Q

relaxation in smooth muscle

A

calcium needs to be removed!
1. Ca-ATPase pumps Ca back into CR
2. Ca unbinds from CaM, decreases MLCK activity
3. myosin phosphatase removes phosphate from myosin, decreases myosin ATPase activity
4. less myosin ATPase activity = decreased muscle tension

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50
Q

latch mechanism

A

smooth muscle can maintain contraction with minimal expenditure of energy

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51
Q

tension in smooth muscle

A

tension development is slowest
cross bridge cycle works more slowly and is not constant

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52
Q

factors influencing smooth muscle activity

A
  • spontaneous electrical activity
  • norepinephrine and acetylcholine)
  • hormones
  • stretch
  • paracrines
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53
Q

goal of cardiovascular system

A

maintain delivery of oxygen and nutrients
removal of wastes from tissue

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54
Q

total blood volume

A

about 5 liters

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55
Q

plasma volume

A

55%

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56
Q

white cell volume

A

less than1%

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57
Q

red cell volume (hematocrit)

A

45%

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58
Q

red cell count

A

5 million

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59
Q

white cell count

A

several thousand

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60
Q

hemoglobin volume

A

15 g/dL

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61
Q

plasma

A

mostly water
gases, nutrients, wastes
hormones
proteins (7%)

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62
Q

proteins in plasma

A

albumin 4.5 (carrier protein)
globulins 2.5
fibrinogen 0.3

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63
Q

Na+ concentration

A

145 mM

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64
Q

K+ concentration

A

4 mM

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65
Q

Ca2+ concentration

A

2.5 mM

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66
Q

CO2 concentration

A

2 ml/100ml (1 mM)

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67
Q

O2 concentration

A

0.2ml/100ml (0.1 mM)

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68
Q

N2 concentration

A

0.9ml/100ml(0.5mM)

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69
Q

glucose concentration

A

100 mg/100ml (5.6 mM)

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70
Q

erythrocytes

A

red blood cells
purpose: deliver oxygen
7 microns in diameter (capillaries are same)
2 mil hemoglobin per RBC (15g/100ml)
no nucleus or ribosomes

71
Q

erythropoietin

A

hormone released by kidney
stimualtes production of red blood cells through negative feedback
decreased O2 in kidneys
kidneys release erythropietin
acts on bone marroe to increase production of hemoglobin
increase O2 delivery to kidney

72
Q

anemia

A

decreased oxygen carrying capacity of blood
can be related to too few red blood cells
or not enough hemoglobin per RBC

73
Q

iron and blood

A

iron is essential for RBC synthesis

74
Q

leukocytes vs erythrocytes

A

leukocytes are larger
less leukocytes than erythrocytes

75
Q

general organization of cardiovascular system

A

right heart pumps to lungs (pulmonary circuit) which pumps to left heart
left heart pumps to tissues (systemic circuit)

76
Q

blood flow

A

pressure/resistance
increase pressure, increase flow
decrease resistance, increase flow

77
Q

resistance to flow

A

viscocity
length
radius (major factor)

78
Q

hemostasis

A

clotting process
essential for preventing blood loss from damaged vessels

79
Q

valves

A

allow for unidirectional flow
passive due to pressure

80
Q

aortic valves

A

tricuspid (right)
bicuspid/mitral (left)
prevent blood from flowing backwards from the ventricle into atria during ventricular contraction

81
Q

semilunar valves

A

pulmonary (right)
aortic (left)
prevent blood from flowing backwards from the aorta and pulmonary artery into ventricles

82
Q

pericardium

A

sac of connective tissue around pericardial fluid

83
Q

endocardium

A

chambers of heart are lined with epithelium

84
Q

myocardium

A

heart muscle

85
Q

cardiac muscle arrangement

A

spiral–> allows ventricular contraction to squeeze blood upward

86
Q

intercalated disks cardiac muscle

A

contain desmosomes that transfer force from cell to cell
also contains gap junctions that allow electrical signals to pass rapidly from cell to cell

87
Q

types of cardiac cells

A

contractile
autorhythmic (pacemaker)

88
Q

contractile cells

A

muscle cells
myocites

89
Q

pacemaker cells

A

in right atrium in SA node
spontaneous

90
Q

cardiac myocyte contraction

A
  1. action potential spreads
  2. voltage gated Ca channels open
  3. Ca causes Ca release from RyR channels
  4. local release causes Ca spark
  5. summed Ca sparks create Ca signal
  6. Ca ions bind to troponin = initiate contraction
91
Q

cardiac myocyte relaxation

A
  1. calcium unbinds from troponin
  2. Ca pumped back into SR
  3. Ca is exchanged with Na
  4. Na gradient is maintained by Na-K-ATPase
92
Q

ventricular myocyte action potential

A
  1. rest: 90 mV
  2. depolarizing phase: increase Na
  3. plateau phase : decrease Na and K, increase Ca (250 msec)
  4. repolarizing phase: increase K, decrease Ca
93
Q

SA node pacemaker action potential

A
  1. rest: -60 mV
  2. slow influx of Na+ (funny current)
  3. depolarization: rapid influx of Ca
  4. repolarization: increase K+ to rest -60 mV
    100 cycles/min
94
Q

SA node pacemaker action potential steps

A
  1. SA node depolarizes
  2. electrical activity goes to AV node
  3. depolarization spreads slowly across atria
  4. depolarization moves rapidly through ventricular system
  5. depolarization wave spreads from apex
95
Q

skeletal muscle
membrane potential
events leading to threshold
rising phase of action potential
repolarization phase
hyperpolarization
duration
refractory period

A

-90 mV
Na+ entry through Ach channels
Na+ entry
rapid, caused by K+ efflux
due to K+ efflux and high K_ permeability
short (1-2msec)
brief

96
Q

contractile myocardium
membrane potential
events leading to threshold
rising phase of action potential
repolarization phase
hyperpolarization
duration
refractory period

A

-90 mV
depolarization enters via gap junctions
Na+ entry
extended plataeu caused by Ca+ entry
no hyperpolarization
extended (200 msec)
long because resetting Na+ gets delayed until end of ap

97
Q

autorhythmic myocardium (Pacemaker)
membrane potential
events leading to threshold
rising phase of action potential
repolarization phase
hyperpolarization
duration
refractory period

A

-60 mV
net Na+ entry through funny channels, reinforced by Ca entry
Ca2+ entry
rapid, caused by K+ efflux
no hyperpolarization
150 msec
no refractory period

98
Q

cardiac cycle

A

late diastole
atrial systole
isovolumetric ventricular contraction
ventricular ejection
isovolumic ventricular relaxation

99
Q

late diastole

A

step 1
both sets of chambers are relaxed
ventricles fill passivley

100
Q

atrial systole

A

step 2
atrial contraction forces small amount of additional blood into ventricles

101
Q

isovolumic ventricular contraction

A

step 3
first phase of ventricular contraction
pushes AV valves closed
doesn’t create enough pressure to open semilunar valves

102
Q

ventricular ejection

A

step 4
ventricular pressure rises and exceeds pressure in arteries
causes semilunar vales to open and blood is ejected

103
Q

isovolumic ventricular relaxation

A

step 5
ventricles relax and pressure decreases
blood flows back into cups of semilunar valves and they close

104
Q

EDV

A

end diastolic volume
diastole is filling

105
Q

ESV

A

end systolic volume
systole is pumping

106
Q

stroke volume

A

amount of blood pumped by one ventricle during a contraction
end diastolic volume - end systoliv volume

107
Q

cardiac outut

A

volume of blood pumped per unit time by left heaart
= heart rate x stroke volume

108
Q

autonomic control of heart

A
  • sympathetic and parasympathetic innervation of SA and AV node
    sympathetic innervates ventricular muscle = regulates force of contraction
109
Q

starling law

A

stroke volume increases as EDV increases

110
Q

funny current

A

sodium leak
causes membrane to slowly depolarize until threshold of ca channels start action potential

111
Q

EKG

A

measures heart rate, electrical signals, duration of ventricular diastole

112
Q

arteries

A

large diameter
low resistance
distribute blood around body
compliant–> keep blood flowing during diastole (elastic recoil)

113
Q

pulse pressure

A

systolic pressure minus diastolic pressure

114
Q

mean arterial pressure

A

diastolic pressure + 1/3 pulse pressure

115
Q

at factors influence pulse pressure

A

stroke volume
heart rate
arterial compliance

116
Q

sphygmomanometry

A

measurement of arterial blood pressure

117
Q

arterioles

A

major source of resistance
drop in pressure
decreased diameter increases resistance
increase resistance decreases flow

118
Q

myogenic tone

A

muscle tone in arterioles

119
Q

local mechanisms of myogenic tone

A

active hyperemia
flow autoregulation

120
Q

active hyperemia

A

increase metabolites
decrease oxygen
increase dilation of arteroile
increase blood flow

121
Q

flow autoregulation

A

decrease pressure
decrease flow
decrease o2, increase metabolies
dilate arteriole
restore normal blood flow

122
Q

neural controls of myogenic tone

A

vasoconstrictors:
sympathetic nerves that release norepinephrine
vasodilators:
neurons that release nitric oxide

123
Q

alpha receptors on muscles

A

constrictor
norepinephrine from sympathetic neurons

124
Q

beta receptors on muscles

A

dilator
epinephrine from adrenal medulle

125
Q

arteriole diameter control

A

release of norepinephrine
sympathetic releases norepinephrine and act on alpha receptor
causes blood vessel to constrict
(decrease NE cause dilate)

126
Q

norepinephrine (a-recpetors)
role
source
type

A

vasoconstriction
baroreceptor and more
sympathetic neurons
neurotransmitter

127
Q

vasopressin
role
source
type

A

vasoconstriction
increase blood pressure in hemorrhage
posterior pituitary
neurohormone

128
Q

angiotensin II
role
source
type

A

vasoconstriction
increase blood pressure
plasma hormone
hormone

129
Q

epinephrine (B-receptors)
role
source
type

A

vasodilation
increase blood flow
adrenal medulla
neurohormone

130
Q

nitric oxide
role
source
type

A

vasodilation
local control blood flow
endothelium
paracrine

131
Q

decrease O2, increase CO2
role
source
type

A

vasodilation
increase blood flow
cell metabolism
paracrine

132
Q

adenosine
role
source
type

A

vasodilation
increase blood flow
hypoxic cells
paracrine

133
Q

histamine
role
source
type

A

vasodilation
increase blood flow
mast cells
paracrine

134
Q

natriuretic peptide (ANP)
role
source
type

A

vasodilation
reduce blood pressure
atrial myocardium
hormone, neurotransmitter

135
Q

dicrotic notch

A

as blood pressure is falling, there is a little bump up

136
Q

atherosclerosis

A

plaque build up
makes walls less compliant
increase pulse pressure

137
Q

capillaries

A

site of exchange between circulatory system and interstitial fluid
small diameter but combined has large total cross sectionl area
= slowest velocity

138
Q

continuous capillaries

A

leaky junctions
endothelial cell junctions allow water and small solutes to pass

139
Q

fenestrated capillaries

A

have large pores
transcytosis brings proteins and macromolecules across endothelium

140
Q

function of lymphatic system

A

return fluid to CVS
clearing proteins from interstitial fluid
absorb fat in intestine
immune system

141
Q

edema

A

accumulation of fluid in interstitial fluid

142
Q

what causes edema

A
  • lymphatic drainage is compromised : accumulate fluid
  • balance of pressure between capillary hydrostatic and somatic pressure may favor movement of fluid into interstitial space
143
Q

what causes pressure favoring movement into interstitial space

A
  • increased capillary pressure
  • decreased plasma protein conc. (liver failure)
  • increased interstitial fluid protein
144
Q

venules and veins

A

return blood to heart
low resistance
pressure is low coming out of the capillaries

145
Q

factors that assist with return of blood to heart

A

valves
skeletal muscle pump
respiratory pump

146
Q

skeletal muscle pump

A

skeletal muscle contracts
squeeze veins in muscle
push blood out
valves make sure its towards heart

147
Q

respiratory pump

A

breathing changes pressure in thoracic cavity
valves make sure pump blood toward heart

148
Q

veins

A

low resistance
very compliant
stretch to accomodate blood volume

149
Q

lymphatic system

A

series of tubes open at one end to interstitial fluid
small lymphatic vessels merge to larger vessels, which open into vena cava
lymph nodes throughout lymphatic system
3L/day of fluid lost from capillaries that enter lymphatic vessels, return to blood stream

150
Q

lymph fluid

A

fluid found in vessels
fluid moves from interstitial fluid to small lymphatic vessels by passive pressure
valves ensure flow is unidirectional

151
Q

lymph fluid

A

fluid found in vessels
fluid moves from interstwhy is blood flow through capillaries constantitial fluid to small lymphatic vessels by passive pressure
valves ensure flow is unidirectional

152
Q

why is blood flow through capillaries constant?

A

resistance of arteries

153
Q

pressure gradient in capillaries

A

diminishes along length of capillary because pressure falls due to resistance

154
Q

baroreceptor reflex

A

negative feedback
increase blood pressure –> baroreceptors fire
decrease sympathetic output
increase parasympathetic output

155
Q

tion of baroreceptors

A

carotid sinus
aortic arch

156
Q

orthostatic hypotension

A

blood pressure decreases when standing
carotid and aortic receptors increase sympathetic output to vasoconstrict
increase resistance
increase blood pressure

157
Q

angiotensin

A

produced in blood by renin (enzyme release in kidney)
kdieny acts on angiotensinogen (Made in liver)

158
Q

angiotensin I

A

10 amino acid
generated from angiotensin
rapidly converted to angiotensin II
converted by ACE

159
Q

ACE

A

angiotensin converting enzyme
found in membrane of epithelial cells in pulimonary capillaries
convert Ang 1 to Ang II

160
Q

angiotensin II

A

8 amino acid
increase blood pressure
constrict arterioles

161
Q

renin secretion

A

decreases arterial pressure
decreased renal perfusion

162
Q

hemorrhage

A

blood loss
increase sympathetic activity
increase blood pressure
increase CO and resistance

163
Q

hemorrhage

A

blood loss
increase sympathetic activity
increase blood pressure
increase CO and resistance

164
Q

hypertension (high blood pressure)
fix

A
  • beta1 antagonist (lower blood pressure by decreasing CO)
  • lower ACE
  • alpha antagonist: block sympathetic vasoconstriction
  • calcium channel blockers: reduce vascular smooth muscle contraction
    diuretics: reduce blood flow and CO
165
Q

calcium source
skeletal vs smooth

A

skeletal: sarcoplasmic reticulum
smooth: extracellular

166
Q

PQ interval (PR)

A

time required for atrial depolarization and action potential to reach ventricles

167
Q

PQ segment

A

time for atrial depolarization to propagate through ventricles

168
Q

ST segment

A

time between ventricular depolarization and repolarization

169
Q

QT interval

A

time required for ventricular depolarization and repolarization

170
Q

RR interval

A

accurate measure of the time of a single cardiac cycle

171
Q

P wave

A

atrial depolarization

172
Q

QRS

A

ventricular depolarization

173
Q

T

A

ventricular repolarization

human physiology (5 decks)

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